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Saturday, August 20, 2011

Dizziness & Vertigo

The most frequent complaints among OPD Dizziness-imbalance,headache,back pain, fatique,Mostly benign,Analyse correctly the nature of disturbance and anatomic location,A feeling of rotation,whirling,non-rotatory swaying,weakness,faintness,unsteadiness,Dizziness may mean giddiness,light head- edness,unsteadiness,swimminess,vertigo.

The specific qualities of vertigo : all subject ive and objective illusion of motion/position
Pseudo vertigo : non-rotatory giddiness
n  Bipolar
¨  Peripheral terminate in hair cells crista ampu llaris SCC & macula acusticae Saccule-Utricle
¨  Central via internal auditory meatus+cochlear + 7th, terminate in the vestibular nuclei (sup-Bechterew, lat-Deiters, med-Schwalbe, inf).  Some fibre from SCC project directly to the flocculonodular lobe+ adjacent vermian cortex cerebellum via the juxtarestiform body 
SCC horizontal is inclined upwards 30° from the horizontal plane, detect turning
The utricle is a gravity-operated receptor which responds to tilting (out of position R)
The saccule responds to acceleration
The utricle-saccule system provides inform ation leading to correct vertical postures when sits,stands and walks
¨  Efferent fiber from cerebellum to i.l. vestibular and fastigial nucleus
¨  Efferent fiber from fastigial ncl to c.l. vestibular nuclei via juxtarestiform body
¨  Lateral and medial nuclei have important connection with the spinal cord via the uncrossed lateral vestibulospinal tract (limb muscles) and via the crossed and uncrossed medial vestibulospinal tract (axial muscles)
¨  Superior and medial nuclei influence 3rd 4th 6th CN 
¨  All vestibular nuclei have afferent and efferent connections with pontin RF à subserve Vestibulo Ocular (clear vision) and Vestibulo Spinal reflex (stable posture)
¨  There are projection from the vestibular nuclei to Cerebral Cortex (intra parietal sulcus and superior Sylvian gyrus)

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INFARCTION STROKE


INFARCTION STROKE
MECHANISM OF ISCHEMIC INFARCTION
  1. Thrombotic
Ø  Thrombotic infarction occurs when a thrombus superimposed on an atherosclerotic plaque
Ø  May be precipitated by an abnormality of blood cloting
  1. Embolic
Ø  Occlusion of an arteri by an embolus
  1. Hemodynamic
Ø  Severe stenosis or occlusion of the proximal arteries
Ø  Collateral compensatory blood flow is inadequate
Ø  Global cerebral perfusion is critically decreased          ( e.g. cardiac output decreased )
CLINICAL CATEGORIES
  1. Atherothrombotic infarction
Ø  Medical history è one or more risk factors
Ø  Headache and vomiting are unusual
Ø  The onset come rapily, may continue to worse over hours or days
Ø  The trombus is superimposed on the atherosclerotic plaque
Ø  Atherosclerotic plaque è extracranial or intracranial arteries
Ø  There are 2 mechanisms :
a.       Atherosclerotic plaque enlarge è stenotic / occlusion
b.      Embolism or plaque fragments è occlusion ( artery – to – artery embolus )
CLINICAL CATEGORIES
  1. Cardioembolic
Ø  The onset is rapid, focal deficit completely and may worsening
Ø  Usually at activity
Ø  The source of embolus :
ü  Cardiac conditions :
v  Atrial fibrillation, acute myocardial infarction, congestive heart failure, mitral or aortic valve disease
ü  Transcardiac conditions ( paradoxical embolus )
v  Right to left cardiac shunt
v  The source of clot : peripheral venous thrombus
Ø  Sometimes clinical finding; isolated homonymous hemianopsia or isolated aphasia
Ø  Brain imaging :
ü  Involve the cortex, commonly in the distribution of branches of the MCA
ü  Possible haemmorhage infarction
  1. Lacunar infarction
Ø  Small lesions, involvement of deep, small, penetrating arteries
Ø  The arteries to branch at 900 ( e.g. lenticulostriate arteries and brain stem )
Ø  The causes are :
ü  Poor collateral connection
ü  Blood obstruction by arterial disease
ü  Thrombus
ü  Embolus

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